Food contamination and cardiovascular disease: a narrative review.

Cardiovascular disease is a significant cause of morbidity and mortality among non-communicable diseases worldwide. Evidence shows that a healthy dietary pattern positively influences many risk factors of cardiometabolic health, stroke, and heart disease, supported by the effectiveness of healthy diet and lifestyles for the prevention of CVD. High quality and safety of foods are prerequisites to ensuring food security and beneficial effects. Contaminants can be present in foods mainly because of contamination from environmental sources (water, air, or soil pollution), or artificially introduced by the human. Moreover, the cross-contamination or formation during food processing, food packaging, presence or contamination by natural toxins, or use of unapproved food additives and adulterants. Numerous studies reported the association between food contaminants and cardiovascular risk by demonstrating that (1) the cross-contamination or artificial sweeteners, additives, and adulterants in food processing can be the cause of the risk for major adverse cardiovascular events and (2) environmental factors, such as heavy metals and chemical products can be also significant contributors to food contamination with a negative impact on cardiovascular systems. Furthermore, oxidative stress can be a common mechanism that mediates food contamination-associated CVDs as substantiated by studies showing impaired oxidative stress biomarkers after exposure to food contaminants.This narrative review summarizes the data suggesting how food contaminants may elicit artery injury and proposing oxidative stress as a mediator of cardiovascular damage.

Hepatic steatosis, carotid atherosclerosis and metabolic syndrome: the STEATO Study.

PURPOSE: Hepatic steatosis is frequently observed in subjects with metabolic syndrome (MS). In type 2 diabetics, it is independently associated with cardiovascular diseases. In order to confirm and extend this finding, a large group of patients with risk factors for atherosclerosis was studied. METHODS: Carotid atherosclerosis was investigated by echo-Doppler, and hepatic steatosis by ultrasound and transaminase values. Strict exclusion criteria were chosen in order to avoid secondary forms of fatty liver and interference on transaminase values. RESULTS: Among 970 enrolled patients, about 20% were diabetics, half had MS and 76% presented echographic hepatic steatosis. In multivariate analyses, fatty liver and MS were associated with carotid atherosclerosis [odds ratio (95% confidence intervals) 2.15 (1.27-3.63) and 1.72(1.12-2.64), respectively], whereas HOMA index was not. Aspartate aminotransferase and alanine aminotransferase were not independently associated with carotid atherosclerosis, whereas gamma-glutamyl transferase showed a link with atherosclerosis beyond MS and steatosis presence. The analyses of the 780 non diabetics recruited showed similar results. CONCLUSIONS: The results of the present study demonstrate that hepatic steatosis measured by echography is associated with carotid atherosclerosis in a large population mostly carrying cardiovascular or metabolic risk factors, independently of MS, cardiovascular diseases, diabetes mellitus and/or insulin resistance.

Effect of anti TNFalpha therapy on arterial diameter and wall shear stress and HDL cholesterol.

It has been recently hypothesized that both TNFalpha and anti TNFalpha treatment have a stimulating effect on nitric oxide synthesis and release. Moreover, an in vitro experiment has demonstrated that HDL-cholesterol binds TNFalpha. Aims of our study were to investigate wall shear stress of peripheral arteries and endothelial function of brachial artery in subjects with Rheumatoid Arthritis (RA) at baseline and after infliximab. Moreover, we evaluated the effect of anti TNFalpha therapy on lipid profile. Ten patients with RA received infliximab therapy at weeks 0, 2 and 6. Lipids and vascular parameters were measured before and the day after each infusion. After the first treatment, FMD increased (3.7 +/- 1.9% versus 17.5 +/- 2.9%, P <0.01) and common carotid and brachial artery diameters decreased (5.9 +/- 0.2 mm versus 5.5 +/- 0.2 mm; 3.5 +/- 0.4 mm versus 3.1 +/- 0.4 mm, respectively, P <0.005). Common carotid and brachial artery wall shear stress increased (21.1 +/- 1.1 dynes/cm2 versus 23.9 +/- 1.4 dynes/cm2; 42.0 +/- 4.7 dynes/cm2 versus 51.6 +/- 5.7 dynes/cm2, P <0.01). Similar results were observed after the second and third infusion. All these parameters returned to pre-treatment level at the following infusion. HDL-cholesterol and apolipoprotein AI significantly decreased after each treatment (1st treatment: 1.4 +/- 0.05 mmol/L versus 1.2 +/- 0.06 mmol/L, P <0.01; 1.73 +/- 0.05 g/L versus 1.57 +/- 0.02 g/L, P <0.03). The present data show vasoconstriction and an increase of wall shear stress in studied arteries after infliximab. HDL cholesterol is reduced by treatment and does not seem to influence FMD.